Pulmonary surfactant is synthesized by alveolar type II cells, stored in the cell in lamellar bodies, and secreted into the alveolar space in a precursor form (tubular myelin), from where it spreads throughout the entire alveolar surface and attains its ability to decrease surface tension. Surfactant is 85% to 90% lipids, predominantly phospholipids, and 10% to 15% proteins (
Table 21.2). The major phospholipid is phosphatidylcholine, approximately 75% of which is present as dipalmitoyl phosphatidylcholine (DPPC). DPPC decreases surface tension and is the major surfaceactive component in surfactant. The second most abundant phospholipid is phosphatidylglycerol, which accounts for •Fig. 21.10 Surface Forces in a Sphere Attempt to Reduce the Area of the Surface and Generate Pressure Within the Sphere. ByLaplace’slaw,thepressuregeneratedisinverselyproportionaltotheradiusofthesphere.A, Intheabsenceofsurfactant,surfaceforcesinthesmallerspheregeneratehigherpressure(heavier purple arrows) thandothoseinthelargersphere(lighter purple arrows). Asaresult,airmovesfromthesmallsphere(higherpressure)tothelargersphere(lowerpressure;black arrow).Thiscausesthesmallspheretocollapseandthelargespheretobecomeoverdistended.B, Surfactant(shaded layer) lowerssurfacetensionandlowersitmoreinthesmallerspherethaninthelargersphere.Thenetresultsarethatthepressuresinthesmallandlargerspheresaresimilar,andthevolumesofthespheresarestabilized.
1% to 10% of total surfactant. These lipids are important in formation of the monolayer on the alveolarair interface, and phosphatidylglycerol is important in the spreading of surfactant over a large surface area. Surfactant protein A, which is the protein most studied, is expressed in alveolar type II cells and in Clara cells in the lungs. Surfactant protein A is involved in the regulation of surfactant turnover, in immunoregulation within the lungs, and in the formation of tubular myelin.
Surfactant is secreted into the airway through exocytosis of the lamellar body by constitutive and regulated mechanisms. Numerous agents, including βadrenergic agonists, activators of protein kinase C, leukotrienes, and purinergic agonists, stimulate the exocytosis of surfactant. The major routes of clearance of pulmonary surfactant within the lung are reuptake by type II cells, absorption into the lymphatic vessels, and clearance by alveolar macrophages. Surfactant is readily inactivated by hypoxia, infection, and edema fluid, which results in a decrease in lung compliance.
In addition to surfactant, another mechanism, interdependence, contributes to stability of the alveoli. Alveoli, except for those on the pleural surface, are surrounded by other alveoli. The tendency of one alveolus to collapse is opposed by the traction exerted by the surrounding alveoli. Thus collapse of a single alveolus causes stretching and distortion of the surrounding alveoli, which in turn are connected to other alveoli. Small openings (pores of Kohn) in the alveolar walls connect adjacent alveoli, whereas the canals of Lambert connect the terminal airways to adjacent alveoli. The pores of Kohn and the canals of Lambert provide collateral ventilation and prevent alveolar collapse (atelectasis).